Hi Pattarawut,

The potential for 'live low - train high', so called intermittent hypoxic training (IHT), to increase high-intensity, anaerobic performance has recently been highlighted in an excellent review by McLean et al. (Sports Med 2014).

There is evidence in literature to indicate that IHT enhances glycolytic enzymes, glucose transport and pH-handling (Vogt et al., JAP 2001; Zoll et al., JAP 2006, Faiss et al., PLoS ONE 2013; Puype et al., MSSE 2013). 

The major mechanisms involved are thought to be HIF-1 activation and greater glycolytic energy turnover during IHT.

Only few studies also evaluated high-intensity or anaerobic performance following IHT. Yet, there is some evidence to support that IHT induces greater improvements in anaerobic power, RSA and YO-YO Intemittent Recovery Test performance than the same training at sea-level (Hendriksen et al., EJAP 2003; Hamlin et al., SJMSS 2010; Faiss et al., PLoS ONE 2013; Galvin et al., BJSM 2013).

Cheers,

Stefan

In my openion 'live low and train high' only improves aerobic metabolism and endurance performance. in contrast for unaerobic metabolism or sprint interval performance competiting in high altitude will improve the overall result

reference: all mexico olympics sprint event results

I think living high would have a better and longer effect in acclimatization, athtles can live in chambers at 3800 m and next day train at sea level, intermitent hypoxia will do its part.

Cheers

Hi Pattarawut,

The potential for 'live low - train high', so called intermittent hypoxic training (IHT), to increase high-intensity, anaerobic performance has recently been highlighted in an excellent review by McLean et al. (Sports Med 2014).

There is evidence in literature to indicate that IHT enhances glycolytic enzymes, glucose transport and pH-handling (Vogt et al., JAP 2001; Zoll et al., JAP 2006, Faiss et al., PLoS ONE 2013; Puype et al., MSSE 2013). 

The major mechanisms involved are thought to be HIF-1 activation and greater glycolytic energy turnover during IHT.

Only few studies also evaluated high-intensity or anaerobic performance following IHT. Yet, there is some evidence to support that IHT induces greater improvements in anaerobic power, RSA and YO-YO Intemittent Recovery Test performance than the same training at sea-level (Hendriksen et al., EJAP 2003; Hamlin et al., SJMSS 2010; Faiss et al., PLoS ONE 2013; Galvin et al., BJSM 2013).

Cheers,

Stefan

I fully agree with Dr Kulandaivelan S regarding the increase in muscle fibers oxidative capacity in line with the major mechanisms involved through the HIF-1 activation as also pointed out by  Dr Stefan De Smet, who instead, relates anaerobic capacity with increased glycolytic enzyme activity. However the question may be anticipated by knowing that  HIF-1a is a transcriptor of three genes EPO, VEGF and mioglobin, mostly related to increased vascular permeability, and haemoglobin oxygen transport up-regulating muscle fibers oxidative capacity 

Thank you very much for your great suggestion.

Hi Dr Pinto,

Thank you for your comment.

There is, indeed, evidence that hypoxic supplementation to training evokes specific muscle remodeling in favour of oxidative metabolism, as for instance a greater increase in capillary density, mitochondrial density, CS activity and markers of mitochondrial biogenesis and metabolism (Terrados et al., JAP 1990; Melissa et al., MSSE 1997; Vogt et al., JAP 2001; Geiser et al., IJSM 2001, Zoll et al., JAP 2006; Schmutz et al., Exp Physiol 2010; Desplanches et al., EJAP 2013; Kon et al., Physiol Rep 2014).

However, Pattarawut raised the question whether IHT would mediate greater improvements in anaerobic performance and its underlying mechanism, for which scarce evidence is presented in my previous post.

VEGF, EPO and myoglobin are indeed downstream targets of HIF-1. However, HIF-1 is known to control the expression of hundreds of genes, among which most of the glycolytic enzymes as well (Porporato et al., FPHAR 2011). Moreover, HIF-1 plays a key role in regulating the switch from aerobic to anaerobic metabolism whenever cells are exposed to hypoxia (Seagroves et al., Mol Cell Biol 2001; Kim et al., Cell Metab 2006; Porporato et al., FPHAR 2011).

In other words, adaptations to maintain oxygen homeostasis are related to increased oxygen delivery (VEGF, EPO, …), as well as decreased oxygen consumption via upregulation of the glycolytic metabolism. They do not rule each other out...

Cheers,

Stefan